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慢性肾病患者饮食中盐摄入量的改变

Altered dietary salt intake for people with chronic kidney disease.

作者信息

McMahon Emma J, Campbell Katrina L, Bauer Judith D, Mudge David W

机构信息

Nutrition and Dietetics, Princess Alexandra Hospital, 199 Ipswich Road, Woolloongabba, Queensland, Australia, 4102.

出版信息

Cochrane Database Syst Rev. 2015 Feb 18(2):CD010070. doi: 10.1002/14651858.CD010070.pub2.

Abstract

BACKGROUND

Salt intake shows great promise as a modifiable risk factor for reducing heart disease incidence and delaying kidney function decline in people with chronic kidney disease (CKD). However, a clear consensus of the benefits of reducing salt in people with CKD is lacking.

OBJECTIVES

This review evaluated the benefits and harms of altering dietary salt intake in people with CKD.

SEARCH METHODS

We searched the Cochrane Renal Group's Specialised Register to 13 January 2015 through contact with the Trials' Search Co-ordinator using search terms relevant to this review.

SELECTION CRITERIA

We included randomised controlled trials (RCTs) that compared two or more levels of salt intake in people with any stage of CKD.

DATA COLLECTION AND ANALYSIS

Two authors independently assessed studies for eligibility and conducted risk of bias evaluation. Results were expressed as risk ratios (RR) and their 95% confidence intervals (CI) for dichotomous outcomes, and mean difference (MD) and 95% CI for continuous outcomes. Mean effect sizes were calculated using the random-effects models.

MAIN RESULTS

We included eight studies (24 reports, 258 participants). Because duration of the included studies was too short (1 to 26 weeks) to test the effect of salt restriction on endpoints such as mortality, cardiovascular events or CKD progression, changes in salt intake on blood pressure and other secondary risk factors were applied. Three studies were parallel RCTs and five were cross-over studies. Selection bias was low in five studies and unclear in three. Performance and detection biases were low in two studies and unclear in six. Attrition and reporting biases were low in four studies and unclear in four. One study had the potential for high carryover effect; three had high risk of bias from baseline characteristics (change of medication or diet) and two studies were industry funded.There was a significant reduction in 24 hour sodium excretion associated with low salt interventions (range 52 to 141 mmol) (8 studies, 258 participants: MD -105.86 mmol/d, 95% CI -119.20 to -92.51; I(2) = 51%). Reducing salt intake significantly reduced systolic blood pressure (8 studies, 258 participants: MD -8.75 mm Hg, 95% CI -11.33 to -6.16; I(2) = 0%) and diastolic blood pressure (8 studies, 258 participants: MD -3.70 mm Hg, 95% CI -5.09 to -2.30; I(2) = 0%). One study reported restricting salt intake reduced the risk of oedema by 56%. Salt restriction significantly increased plasma renin activity (2 studies, 71 participants: MD 1.08 ng/mL/h, 95% CI 0.51 to 1.65; I(2) = 0%) and serum aldosterone (2 studies, 71 participants: 6.20 ng/dL (95% CI 3.82 to 8.58; I(2) = 0%). Antihypertensive medication dosage was significantly reduced with a low salt diet (2 studies, 52 participants): RR 5.48, 95% CI 1.27 to 23.66; I(2) = 0%). There was no significant difference in eGFR (2 studies, 68 participants: MD -1.14 mL/min/1.73 m(2), 95% CI -4.38 to 2.11; I(2) = 0%), creatinine clearance (3 studies, 85 participants): MD -4.60 mL/min, 95% CI -11.78 to 2.57; I(2) = 0%), serum creatinine (5 studies, 151 participants: MD 5.14 µmol/L, 95% CI -8.98 to 19.26; I(2) = 59%) or body weight (5 studies, 139 participants: MD -1.46 kg; 95% CI -4.55 to 1.64; I(2) = 0%). There was no significant change in total cholesterol in relation to salt restriction (3 studies, 105 participants: MD -0.23 mmol/L, 95% CI -0.57 to 0.10; I(2) = 0%) or symptomatic hypotension (2 studies, 72 participants: RR 6.60, 95% CI 0.77 to 56.55; I(2) = 0%). Salt restriction significantly reduced urinary protein excretion in all studies that reported proteinuria as an outcome, however data could not be meta-analysed.

AUTHORS' CONCLUSIONS: We found a critical evidence gap in long-term effects of salt restriction in people with CKD that meant we were unable to determine the direct effects of sodium restriction on primary endpoints such as mortality and progression to end-stage kidney disease (ESKD). We found that salt reduction in people with CKD reduced blood pressure considerably and consistently reduced proteinuria. If such reductions could be maintained long-term, this effect may translate to clinically significant reductions in ESKD incidence and cardiovascular events. Research into the long-term effects of sodium-restricted diet for people with CKD is warranted, as is investigation into adherence to a low salt diet.

摘要

背景

盐摄入作为一种可改变的风险因素,在降低慢性肾脏病(CKD)患者心脏病发病率和延缓肾功能衰退方面显示出巨大潜力。然而,对于CKD患者减少盐摄入的益处,目前尚未形成明确共识。

目的

本综述评估了改变CKD患者饮食盐摄入量的益处和危害。

检索方法

我们通过与试验检索协调员联系,使用与本综述相关的检索词,检索了截至2015年1月13日的Cochrane肾脏组专业注册库。

入选标准

我们纳入了比较CKD任何阶段患者两种或更多盐摄入量水平的随机对照试验(RCT)。

数据收集与分析

两位作者独立评估研究的入选资格并进行偏倚风险评估。结果以二分结局的风险比(RR)及其95%置信区间(CI)表示,连续结局以均值差(MD)和95%CI表示。平均效应量使用随机效应模型计算。

主要结果

我们纳入了八项研究(24篇报告,258名参与者)。由于纳入研究的持续时间过短(1至26周),无法测试盐限制对死亡率、心血管事件或CKD进展等终点的影响,因此应用了盐摄入量变化对血压和其他次要风险因素的影响。三项研究为平行RCT,五项为交叉研究。五项研究的选择偏倚较低,三项研究不明确。两项研究的实施和检测偏倚较低,六项研究不明确。四项研究的失访和报告偏倚较低,四项研究不明确。一项研究存在高残留效应的可能性;三项研究因基线特征(药物或饮食变化)存在高偏倚风险,两项研究由行业资助。低盐干预使24小时钠排泄量显著降低(范围为52至141 mmol)(八项研究,258名参与者:MD -105.86 mmol/d,95%CI -119.20至-92.51;I² = 51%)。减少盐摄入量显著降低收缩压(八项研究,258名参与者:MD -8.75 mmHg,95%CI -11.33至-6.16;I² = 0%)和舒张压(八项研究,258名参与者:MD -3.70 mmHg,95%CI -5.09至-2.30;I² = 0%)。一项研究报告称,限制盐摄入可使水肿风险降低56%。盐限制显著增加血浆肾素活性(两项研究,71名参与者:MD 1.08 ng/mL/h,95%CI 0.51至1.65;I² = 0%)和血清醛固酮(两项研究,71名参与者:6.20 ng/dL(95%CI 3.82至8.58;I² = 0%)。低盐饮食使降压药物剂量显著减少(两项研究,52名参与者):RR 5.48,95%CI 1.27至23.66;I² = 0%)。估算肾小球滤过率(两项研究,68名参与者:MD -1.14 mL/min/1.73 m²,95%CI -4.38至2.11;I² = 0%)、肌酐清除率(三项研究,85名参与者):MD -4.60 mL/min,95%CI -11.78至2.57;I² = 0%)、血清肌酐(五项研究,151名参与者:MD 5.14 µmol/L,95%CI -8.98至19.26;I² = 59%)或体重(五项研究,139名参与者:MD -1.46 kg;95%CI -4.55至1.64;I² = 0%)无显著差异。与盐限制相关的总胆固醇无显著变化(三项研究,105名参与者:MD -0.23 mmol/L,95%CI -0.57至0.10;I² = 0%)或症状性低血压(两项研究,72名参与者:RR 6.60,95%CI 0.77至56.55;I² = 0%)。在所有将蛋白尿作为结局报告的研究中,盐限制显著降低尿蛋白排泄,但数据无法进行Meta分析。

作者结论

我们发现CKD患者盐限制长期影响方面存在关键证据空白,这意味着我们无法确定钠限制对死亡率和终末期肾病(ESKD)进展等主要终点的直接影响。我们发现CKD患者减少盐摄入可显著降低血压,并持续降低蛋白尿。如果这种降低能长期维持,这种效果可能转化为ESKD发病率和心血管事件的临床显著降低。有必要对CKD患者钠限制饮食的长期影响进行研究,同时也需要研究对低盐饮食的依从性。

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